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LDL‑induced NLRC3 inflammasome activation in cardiac fibroblasts contributes to cardiomyocytic dysfunction

  • Authors:
    • Peng Wang
    • Wenbo Zhang
    • Zhen Feng
    • Jian Zhang
    • Ying Sun
    • Wei Zhang

  • View Affiliations

  • Published online on: May 25, 2021     https://doi.org/10.3892/mmr.2021.12165
  • Article Number: 526

  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Heart failure (HF) is a progressive myocardial disease that affects pulse rate. Notably, chronic inflammation serves a crucial role in cardiac dysfunction and HF. Appropriate cardiomyocyte‑fibroblast communication is essential for cardiac function. In addition, cardiac fibroblasts (CFs) are the main cellular population in the cardiac microenvironment; therefore, determining the role of CFs in HF progression and the associated molecular basis is important. In the present study, ELISAs were performed to detect inflammatory factors in the sera of patients with HF and their association with CF activation was analyzed using Pearson's correlation coefficient. The mechanism underlying the proinflammatory phenotype of CFs was investigated via western blotting. Notably, the levels of IL10 and TNF‑α were significantly increased in the sera of patients with HF. Further analysis revealed that CFs were extensively activated in the cardiac tissues of patients with HF and released excessive amounts of cytokines, which could impair the viability of cardiomyocytes. Moreover, low‑density lipoprotein (LDL)‑induced NLRC3 inflammasome was activated in CFs, which gave rise to proinflammatory phenotypes. Targeting LDL in CFs significantly improved the functioning of cardiomyocytes and inhibited apoptosis. These findings highlighted the critical role of LDL in inflammasome activation; to the best of our knowledge, the present study is the first to reveal that CF‑induced microenvironmental inflammation may suppress cardiomyocyte viability. The present study established the cellular basis for CF activation during HF progression and provided information on the cellular interactions important for HF treatment.
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July-2021
Volume 24 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

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  • Impact Factor: 3.4
  • Ranked Medicine Research and Experimental
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  • CiteScore: 7.6
  • CiteScore Rank: Q1: #82/347 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.647
  • SCImago Journal Rank (SJR): 0.781
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Spandidos Publications style
Wang P, Zhang W, Feng Z, Zhang J, Sun Y and Zhang W: LDL‑induced NLRC3 inflammasome activation in cardiac fibroblasts contributes to cardiomyocytic dysfunction. Mol Med Rep 24: 526, 2021.
APA
Wang, P., Zhang, W., Feng, Z., Zhang, J., Sun, Y., & Zhang, W. (2021). LDL‑induced NLRC3 inflammasome activation in cardiac fibroblasts contributes to cardiomyocytic dysfunction. Molecular Medicine Reports, 24, 526. https://doi.org/10.3892/mmr.2021.12165
MLA
Wang, P., Zhang, W., Feng, Z., Zhang, J., Sun, Y., Zhang, W."LDL‑induced NLRC3 inflammasome activation in cardiac fibroblasts contributes to cardiomyocytic dysfunction". Molecular Medicine Reports 24.1 (2021): 526.
Chicago
Wang, P., Zhang, W., Feng, Z., Zhang, J., Sun, Y., Zhang, W."LDL‑induced NLRC3 inflammasome activation in cardiac fibroblasts contributes to cardiomyocytic dysfunction". Molecular Medicine Reports 24, no. 1 (2021): 526. https://doi.org/10.3892/mmr.2021.12165